MCQ practice : SAAG
03:10 PMOctober 9, 2025

MCQ practice : SAAG


Click here to watch quick trick on SAAG before or after the quiz


1. What is the primary clinical use of the Serum-Ascites Albumin Gradient (SAAG)?

A To differentiate types of jaundice

B To differentiate transudative and exudative ascites

C To assess kidney function

D To diagnose acute pancreatitis

Correct answer : B


2. A patient with ascites has a SAAG of 1.8 g/dL. What is the most likely underlying cause?

A) Malignancy

B) Infection

C) Portal Hypertension

D) Protein-losing enteropathy

Correct answer : C


3. Which condition is typically associated with a low SAAG (<1.1 g/dL)?

A) Congestive Heart Failure

B) Cirrhosis

C) Ovarian Tumor

D) Budd-Chiari Syndrome

Correct answer : C


4. A patient presented with massive abdominal swelling. Paracentesis fluid was sent for lab analysis and results show serum protein to be 3 g/dL and ascitic fluid protein to be 1 g/dL. What is the likely diagnosis?

A) Congestive heart failure

B) Early Budd Chiari syndrome

c) Late Budd Chiari syndrome

D) Tuberculosis

Correct answer : C

Explanation :

Let’s carefully analyze the data:

  • Serum protein: 3.5 g/dL

  • Ascitic fluid protein: 1.5 g/dL

🧮 Serum–Ascites Albumin Gradient (SAAG):

SAAG=Serum protein−Ascitic fluid protein=3.5−1.5=2.0

Since SAAG > 1.1 g/dL, this indicates ascites due to portal hypertension.

Now, we use ascitic fluid total protein to differentiate causes of high SAAG ascites:

CauseSAAGAscitic Fluid Protein (g/dL)
Cirrhosis>1.1<2.5
Congestive Heart Failure (CHF)>1.1>2.5
Early Budd–Chiari>1.1>2.5
Late Budd–Chiari>1.1<2.5
Tuberculosis / Malignancy<1.1>2.5

🔍 Interpretation:

  • SAAG = 2.0 → Portal hypertension present

  • Ascitic fluid protein = 1.5 g/dL → Low protein (<2.5)

This combination (high SAAG + low protein) is characteristic of late Budd–Chiari syndrome.


Pathophysiological Explanation:

  • In early Budd–Chiari, hepatic venous outflow obstruction causes congestion → increased protein leakage → high protein ascites (>2.5 g/dL).

  • As disease progresses to late Budd–Chiari, hepatic fibrosis and cirrhosis develop → liver synthetic dysfunction → ascitic protein levels fall (<2.5 g/dL) though SAAG remains >1.1 g/dL due to persistent portal hypertension.

Thus, in this case:

SAAG > 1.1 + Low ascitic protein → Late Budd–Chiari syndrome


5. A 47 year old male with a BMI of 35 kg/ m2 presents with jaundice, loss of appetite with abdominal pain and increasing abdominal girth over 3–4 weeks. He is teetotal with no other past medical history. He does not take any regular medication. On examination he has hepatosplenomegaly and ascites, with no peripheral oedema.

Full blood count:

Haemoglobin 190 g/L

WCC 13×109/L

Platelets 690×109/L

LFTs:
Bilirubin 72 μmol/L (4.21 mg/dL) ALT 500 U/L
ALP 460 U/L
Albumin 31 g/L
Ascitic fluid albumin 22 g/L

What is the most likely cause of his presentation?

A. Alcoholic liver disease
B. Congestive cardiac failure

C. Haemochromatosis
D. Hepatic vein thrombosis

Correct answer : D

Explanation : The patient has polycythaemia vera causing Budd–Chiari syndrome. The ascitic fluid is an exudate with a serum–ascites albumin gradient (SAAG) of <11 g/L. The other causes listed would have a high SAAG.

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